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1 ing both cI(VP882) DNA binding and cI(VP882) autoproteolysis.
2 uggesting a His-Thr-Thr active triad for the autoproteolysis.
3 human enzyme to be a prerequisite to trigger autoproteolysis.
4 is decrease was found to be due, in part, to autoproteolysis.
5 d the enzyme activity presumably by reducing autoproteolysis.
6 ining an affinity tag and modified to resist autoproteolysis.
7  proceed via mechanisms which do not involve autoproteolysis.
8 mmunoblotting shows that it undergoes normal autoproteolysis.
9 nd stabilization of the CPD, enhancing toxin autoproteolysis.
10                This effect is independent of autoproteolysis.
11 evelopment targeting the C. difficile toxins autoproteolysis.
12 l effect on the LDL receptor, PCSK9 requires autoproteolysis.
13 te binding pocket undergo rearrangement upon autoproteolysis.
14 RO(FUR) when compared to PRO(PC1) to enhance autoproteolysis.
15 ), we proposed a mechanism of intramolecular autoproteolysis.
16 inhibitor or ligand and is poised to undergo autoproteolysis.
17 odule with traits matching those ascribed to autoproteolysis.
18 iated aggregation is above the threshold for autoproteolysis.
19 he bacterial cell surface via intermolecular autoproteolysis.
20  was enhanced substantially by inhibition of autoproteolysis.
21 hereas the C-terminal domain is required for autoproteolysis.
22 vation of amidase activity by intramolecular autoproteolysis.
23 64A conferred significant protection against autoproteolysis.
24 iated adherence is enhanced by inhibition of autoproteolysis.
25 reserved during the folding of GA to trigger autoproteolysis.
26  chelation, suggesting that release involves autoproteolysis.
27 ought to further define the mechanism of Hap autoproteolysis.
28 ominantly a nuclear protease which undergoes autoproteolysis.
29  of respiratory secretions that inhibits Hap autoproteolysis.
30 ered agonist of the receptor, but not on its autoproteolysis, a characteristic biochemical feature of
31 port here a 1.9-A-resolution structure of an autoproteolysis-active precursor (a T152C mutant) that i
32          The p52 fragment has a low level of autoproteolysis activity that possibly increases the aut
33                                     In vitro autoproteolysis allowed the mutant enzymes to be activat
34        This upregulation resulted in limited autoproteolysis and activation of HtrA1.
35 These results highlight the critical role of autoproteolysis and an intermolecular mechanism of cleav
36 ostatin4.5 (AS4.5) is the product of plasmin autoproteolysis and consists of kringles 1 to 4 and appr
37 ities to eukaryotic SEA domains that undergo autoproteolysis and have been implicated in mechanotrans
38 ted signaling of a GPR56 mutant defective in autoproteolysis and hence, in Stachel peptide exposure.
39   In contrast, ASC is critical for caspase-1 autoproteolysis and IL-1beta secretion by the NLRC4, NLR
40 hreonine, which plays a central role in both autoproteolysis and in its amidase activity.
41  that overproduction of BofC inhibits SpoIVB autoproteolysis and leads to a delay in proteolytic clea
42 ke serine protease domain that mediates SltB autoproteolysis and proteolytic cleavage of SltA.
43 nthrax lethal toxin (LeTx)-induced caspase-1 autoproteolysis and speck formation.
44  threshold of Hap precursor was required for autoproteolysis and that this threshold approximated exp
45             This constraint is released upon autoproteolysis and we propose a molecular basis for the
46 p26 segment is generated from p67 due to its autoproteolysis and whether p26 is required for the prot
47 ceptor binding, endocytosis, pore formation, autoproteolysis, and glucosyltransferase-mediated modifi
48 ude of Hap expression, the efficiency of Hap autoproteolysis, and the level of Hap-mediated adherence
49 n cytomegalovirus (CMV), assemblin undergoes autoproteolysis at an internal (I) site located near the
50                              Capsids undergo autoproteolysis at residue 570, generating the 74-residu
51 trast to other caspases, we demonstrate that autoproteolysis at the second cleavage site, Asp316, is
52 IV protease (PR), we noted that it underwent autoproteolysis (autolysis) to give discrete cleavage pr
53 t and to presumably form the active site for autoproteolysis but not for the chemistry of cleavage.
54            These nucleoli lacked significant autoproteolysis, but many nucleolar proteins and autoant
55                                              Autoproteolysis can be abrogated by relief of conformati
56 bstrate with positive cooperativity, and its autoproteolysis can be stimulated with exogenous substra
57 nt proteins released from the large toxin by autoproteolysis catalyzed by an embedded cysteine protea
58  of the nucleoli may attribute to their poor autoproteolysis, causing autologous immune stimulation u
59 across varied pH conditions, indicating that autoproteolysis cleavage is not required for LSV maturat
60  is consistently rescued by co-expression of autoproteolysis-deficient full-length NLRP1.
61 ike proprotein convertases, TIMPs, shedding, autoproteolysis, dimerization, exocytosis, endocytosis,
62 ivation requires a RecA-stimulated repressor autoproteolysis event, with cleavage occurring precisely
63                                       First, autoproteolysis generating intermediate products, at lea
64                 CARD8 undergoes constitutive autoproteolysis, generating an N-terminal (NT) fragment
65                      Kinetic analysis of Hap autoproteolysis in bacteria expressing Hap under control
66 48 cleavage and the functional importance of autoproteolysis in the context of hypovirus replication
67 nts for p29 and p48 cleavage and the role of autoproteolysis in the context of hypovirus replication.
68 nd-generation IP6 analogs designed to induce autoproteolysis in the gut lumen, prior to toxin uptake,
69 A and other S24 peptidases, NG1427 undergoes autoproteolysis in vitro, which is facilitated by either
70 l of an inducible promoter demonstrated that autoproteolysis increases as the density of Hap precurso
71 ructure of a shared protein domain, the GPCR Autoproteolysis INducing (GAIN) domain, has enabled the
72 GPS to be part of a larger domain named GPCR autoproteolysis inducing (GAIN) domain.
73 ately 320-residue domain that we termed GPCR-Autoproteolysis INducing (GAIN) domain.
74 eolysis occurs within the extracellular GPCR autoproteolysis-inducing (GAIN) domain that is proximal
75 led that this antibody targets the CD97 GPCR autoproteolysis-inducing (GAIN) domain, whose presence i
76 mone-binding, and G-protein-coupled receptor autoproteolysis-inducing (GAIN) domains).
77 in-like (PLL) and G protein-coupled receptor autoproteolysis-inducing (GAIN)] in its ECR.
78 n inverse-agonist monobody, revealing a GPCR-Autoproteolysis-Inducing domain and a previously unident
79  contain a modular protease, termed the GPCR autoproteolysis-inducing domain that self-cleaves the re
80                     Most aGPCRs undergo GPCR autoproteolysis-inducing domain-mediated protein cleavag
81  characterized their toxin binding affinity, autoproteolysis induction, and cation interactions.
82                                          cis-Autoproteolysis is a post-translational modification nec
83 and HMGB1 in circulation, although caspase-1 autoproteolysis is abolished.
84                             However, Pim1p's autoproteolysis is intact, and its overexpression restor
85                                          Hap autoproteolysis is mediated by Ser(243) and occurs at LN
86 A two-step dimerization mechanism to trigger autoproteolysis is proposed to accommodate the data pres
87       An obstacle to our understanding of GA autoproteolysis is the uncertainty concerning its quater
88  at the P1 position in the NS3-NS4A (NS3-4A) autoproteolysis junction, while a cysteine is maintained
89                               However, after autoproteolysis, many enzymes, like ThnT, are observed t
90 orms are processed into two peptides through autoproteolysis mediated by the C-terminal domain of hNu
91 s we show that CwpV undergoes intramolecular autoproteolysis, most likely facilitated by a N-O acyl s
92 volved in cell adhesion has a characteristic autoproteolysis motif of HLT/S known as the GPCR proteol
93                  In intact cells, caspase-12 autoproteolysis occurred in the inhibitory complex conta
94 d site-directed mutagenesis established that autoproteolysis occurs at LT1046-7, FA1077-8, and FS1067
95 olytic activity (HapS243A) demonstrated that autoproteolysis occurs by an intermolecular mechanism.
96                                        AGPCR autoproteolysis occurs within the extracellular GPCR aut
97       This insertion results in differential autoproteolysis of ADAMTS17, and thus, predicts altered
98                                              Autoproteolysis of caspase-8 may be a mechanism for incr
99 eolysis activity that possibly increases the autoproteolysis of full-length p67.
100                                              Autoproteolysis of SpoIVB is tightly linked to the initi
101 cteriophage usually involves RecA-stimulated autoproteolysis of the bacteriophage repressor protein.
102 aspase-8 and is followed by specific limited autoproteolysis of the linker which separates the two su
103                   Intracellular LPS-elicited autoproteolysis of these inflammatory caspases leads to
104 ly members is mediated by enzyme-independent autoproteolysis of these SEA-like domains.
105 zymogen serine protease, S1P matures through autoproteolysis of two pro-domains, with one cleavage ev
106  present as a dimer, how can RecA-stimulated autoproteolysis play a role in bacteriophage induction?
107                                     This cis-autoproteolysis possesses unique kinetics characterized
108 proteinase, HTLV-1 proteinase also undergoes autoproteolysis rapidly upon renaturation to produce two
109 ecursor through a series of highly regulated autoproteolysis reactions.
110 est that the model for calpain activation by autoproteolysis requires re-investigation.
111 cal or E. coli RecA proteins or high pH, and autoproteolysis requires the active and cleavage site re
112  Thr/Ser/Cys-152 in activation suggests that autoproteolysis resembles proteolysis by serine/cysteine
113 PKD) proteins constitutes a highly conserved autoproteolysis sequence, but its catalytic mechanism re
114                         Cleavage in the GPCR autoproteolysis site (GPS) is an aGPCR hallmark; thus, w
115 based on a precursor structure paused at pre-autoproteolysis stage by a reversible inhibitor (glycine
116  domain is both necessary and sufficient for autoproteolysis, suggesting an autoproteolytic mechanism
117         The YscP-mediated inhibition of YscU autoproteolysis suggests that the cleavage event may act
118 g temperatures of GA dimers before and after autoproteolysis suggests two states of dimerization in t
119 tic which are more capable of inducing toxin autoproteolysis than the native ligand, warranting furth
120  was hypothesized to be critical for driving autoproteolysis through an N-O acyl shift.
121 imerization of GA plays an essential role in autoproteolysis to activate the amidase activity.
122 surface globular beta-actin mediates plasmin autoproteolysis to AS4.5.
123 iate plasmin binding to the cell surface and autoproteolysis to AS4.5.
124 h NLRP1 and CARD8 undergo post-translational autoproteolysis to generate two non-covalently associate
125 sid and digests the delta domain followed by autoproteolysis to produce the metastable Prohead-II.
126 m a single chain precursor by intramolecular autoproteolysis to yield the N-terminal nucleophile.
127 tivity, and purified Cpl appeared to undergo autoproteolysis upon transfer to inhibitor-free buffer.
128 ns a self-processing module (SPM) undergoing autoproteolysis via an aspartic anhydride.
129                               A mechanism of autoproteolysis via an N-O acyl shift was proposed to re
130 t to promote bacterial aggregation only when autoproteolysis was inhibited, indicating that the thres
131 trast, neither tethered agonist activity nor autoproteolysis were necessary for Lphn2's role as a rep
132                    However, the role of this autoproteolysis, which directly activates executioner ca
133 protease domain (CPD) on the toxin, inducing autoproteolysis, which liberates a virulence factor in t
134                       Then plasmin undergoes autoproteolysis within the inner loop of kringle 5, whic

 
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